Entamoeba histolytica:: Lipid rafts are involved in adhesion of trophozoites to host extracellular matrix components
Entamoeba histolytica:: Lipid rafts are involved in adhesion of trophozoites to host extracellular matrix components
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DOI：
10.1016/j.exppara.2008.06.003
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发表时间：
2008-10-01
影响因子：
2.1
通讯作者：
Temesvari, L. A.
中科院分区：
文献类型：
--
作者：
Mittal, K.;Welter, B. H.;Temesvari, L. A.
阿米巴是引起阿米巴痢疾的病原体，黏附是其重要的致病功能。脂筏是富含胆固醇的区域，在细胞过程的区隔中发挥作用。在溶组织埃希氏菌中，木筏参与了寄生虫-宿主细胞的相互作用；然而，它们在寄生虫-宿主细胞外基质(ECM)相互作用中的作用尚未被探索。用胆固醇萃取剂甲基-β-环糊精(M-β-CD)破坏木筏，会抑制与胶原的黏附，并在较小程度上抑制与纤维连接蛋白的黏附。在MβCD处理的细胞中补充胆固醇，使用脂蛋白-胆固醇浓缩物，恢复了与胶原的粘附性。共聚焦显微镜显示在寄生虫-ECM交界处有丰富的木筏。半乳糖/N-乙酰半乳糖胺抑制凝集素是一种RAFT驻留的粘附素，它通过与宿主糖蛋白上的半乳糖或N-乙酰半乳糖胺部分结合来介导与宿主细胞的相互作用。在这项研究中，半乳糖抑制了与胶原的黏附，但不抑制与纤维连接蛋白的黏附。综上所述，这些数据表明，RAFT参与了溶组织埃希氏菌-ECM的相互作用，RAFT相关的Gal/GalNAc凝集素可能作为胶原蛋白受体。(C)2008 Elsevier Inc.保留所有权利。
Adhesion is an important virulence function for Entamoeba histolytica, the causative agent of amoebic dysentery. Lipid rafts, cholesterol-rich domains, function in compartmentalization of cellular processes. In E. histolytica, rafts participate in parasite-host cell interactions; however, their role in parasite-host extracellular matrix (ECM) interactions has not been explored. Disruption of rafts with a cholesterol extracting agent, methyl-beta-cyclodextrin (M beta CD), resulted in inhibition of adhesion to collagen, and to a lesser extent, to fibronectin. Replenishment of cholesterol in M beta CD-treated cells, using a lipoprotein-cholesterol concentrate, restored adhesion to collagen. Confocal microscopy revealed enrichment of rafts at parasite-ECM interfaces. A raft-resident adhesin, the galactose/N-acetylgalactosamine-inhibitable lectin, mediates interaction to host cells by binding to galactose or N-acetylgalactosamine moieties on host glycoproteins. In this study, galactose inhibited adhesion to collagen, but not to fibronectin. Together these data suggest that rafts participate in E. histolytica-ECM interactions and that raft-associated Gal/GalNAc lectin may serve as a collagen receptor. (C) 2008 Elsevier Inc. All rights reserved.